Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human melanoma cells (MM96E) were incubated with a phenotypic modifier (L-ethionine) to compare its effects on phenotypic expression with those induced by sodium butyrate and dimethyl sulfoxide. In contrast to the latter agents, L-ethionine (8mM) failed to arrest the cell cycle at the G1 phase or to inhibit colony formation ability after 48 hr incubation. Tyrosinase activity changed in parallel with 5-S-cysteinyldopa (5-S-CD) content during treatment with sodium butyrate or dimethyl sulfoxide. Tyrosinase was inhibited in L-ethionine-treated cells, probably because of metabolism of L-ethionine to sulfhydryl compounds; this remains to be clarified. Gamma-glutamyl transpeptidase activity changed inversely with tyrosinase activity after sodium butyrate or dimethyl sulfoxide incubation, whereas L-ethionine did not significantly alter the enzyme activity. In addition, only sodium butyrate induced alkaline phosphatase activity. L-ethionine was less effective than sodium butyrate or dimethyl sulfoxide in inhibiting expression of the B8G3 melanosomal antigen, as determined by Western blotting. These results suggest that phenotypic modifiers (differentiation inducers) affect melanoma cells in various ways and that melanogenesis therefore reflects only one aspect of differentiation in pigment cells.
J Dermatol 1992 Nov
PMID:Alteration of melanoma melanogenesis by phenotypic modifiers. 136 29

Interactions among the cells and matrices of the epidermis and mesenchyme of skin are essential for hair follicle initiation and development. The identification of receptors for epidermal growth factor (EGF) on epithelial components of the follicle during growth has suggested that the ligand participates in some of these events. We have used affinity-purified antibodies together with an alkaline phosphatase detection procedure to investigate the distribution of EGF in the skin of the sheep during wool follicle formation. Immunoreactivity was restricted to the periderm and intermediate layers of fetal epidermis at 55 d of gestation, when the first wave of wool follicles are initiated. This particular distribution persisted during subsequent development but never became associated with the basal cells of the epidermis. The activity was lost around 118 d, coinciding with sloughing of the periderm. No immunoreactivity was found in the plugs or the dermal condensations of the developing follicles. At approximately 105 d of gestation, however, reactions were detected in the outer root sheath as the follicles matured and in the differentiating cells of the sebaceous glands. A similar distribution pattern was also noted at 140 d, just prior to birth, and in adult animals, indicating that EGF was sequestered and perhaps synthesized within the follicle. The presence of immunoreactive material was also associated with the pilary canals and the skin surface, suggesting that this may have had its origin in the sebaceous glands. We examined this using a radioreceptor assay for EGF. Material washed from the skin surface and sebaceous gland extracts were found to displace 125I-EGF from rat liver membranes, in parallel with mouse EGF.
J Invest Dermatol 1992 Jan
PMID:Localization of epidermal growth factor immunoreactivity in sheep skin during wool follicle development. 137 Feb 28

The expression of T6 antigen within hair follicles in alopecia areata was studied using the APAAP technique (alkaline phosphatase monoclonal anti-alkaline phosphatase method). Scalp biopsies were taken from 15 subjects with alopecia areata, nine in an active stage and 6 in a stationary stage of the disease. Six-micrometer-thick frozen sections were stained with OKT6 antiserum. OKT6 are monoclonal antibodies raised against human thymocytes; they cross-react with epidermal Langerhans cells and are a highly specific marker. Nine of the specimens displayed T6 staining on keratinocytes in the bulb matrix, and all nine were from the subjects presenting the active stage of disease. The specimens from the other six biopsies, from subjects in a stationary stage, did not show T6 staining of bulbar keratinocytes. Moreover, in four of the active-stage cases we found T6 staining also on epidermal keratinocytes.
Int J Dermatol 1992 Feb
PMID:Expression of T6 antigen on keratinocytes in alopecia areata. 155 31

Fifty-four patients with cutaneous tuberculosis, consisting of 23 with lupus vulgaris, 22 with scrofuloderma, and nine with verrucosa cutis, were investigated for cell-mediated immunity, through estimation of peripheral total T lymphocytes (CD3+), CD4+ (helper/inducer), and CD8+ (cytotoxic/suppressor) lymphocytes, by immunohistochemical staining of peripheral blood smears, using specific monoclonal antibodies and the alkaline phosphatase-antialkaline phosphatase (APAAP) method. Absolute values of total T lymphocytes (CD3+), and CD4+ and CD8+ subsets, were found to be significantly raised in scrofuloderma, but the percentage values and the CD4+/CD8+ ratio remained unaltered. In tuberculosis verrucosa cutis, only the percentage of the CD8+ subset of T lymphocytes was found to be significantly lowered, and this altered the CD4+/CD8+ ratio. No significant change was observed in the peripheral blood T cells and their subpopulations in patients suffering from lupus vulgaris.
Int J Dermatol 1992 Feb
PMID:Peripheral T lymphocytes and their subsets in cutaneous tuberculosis. 155 33

The influence of recombinant human interferon alpha 2a (rIFN alpha), recombinant human interferon beta 1 (rIFN beta), and recombinant human interferon gamma (rIFN gamma) on human dermal microvascular endothelial cells (HDMEC) cultured in vitro was studied in various rIFN concentrations (0.1 IU/ml-10(4) IU/ml) over 2, 3, 4, 6, 8, and 10 d. Cell morphology and ultrastructure, cell proliferation, expression of class II alloantigens (HLA-DR and HLA-DQ), and intercellular adhesion molecule-1 (ICAM-1) were investigated using an in vitro technique established in our laboratory. All rIFN tested induced alterations of typical HDMEC morphology; the cells became spindle-shaped and fibroblastoid, although they maintained their endothelial cell marker expression. Also, all IFN dose- and time-dependently inhibited the proliferation of HDMEC in vitro (rIFN alpha greater than beta greater than gamma), whereby rIFN alpha exerted the strongest growth-inhibitory effect. Alkaline phosphatase anti-alkaline phosphatase (APAAP) immunocytochemistry of the cultured cells showed dose- and time-dependent stimulation of ICAM-1 and class II antigen expression only by rIFN gamma (HLA-DR greater than HLA-DQ), rIFN alpha and beta did not exert any immunomodulatory activity on HDMEC in vitro. These results indicate that HDMEC are an important target for the action of IFN. Besides growth inhibition, it seems that rIFN gamma in particular may be involved in the modulation of leucocyte adhesion and trafficking by altering the immunophenotype of the endothelial cell population.
J Invest Dermatol 1990 Dec
PMID:Effects of rIFN alpha, beta, and gamma on the morphology, proliferation, and cell surface antigen expression of human dermal microvascular endothelial cells in vitro. 197 80

By means of monoclonal antibodies (mab) and alkaline phosphatase anti-alkaline-phosphatase (APAAP) technique, the distribution and characteristics of lymphocytic infiltrates were studied in biopsies from 15 patients with bullous pemphigoid (b.P.) and 5 patients with pemphigus vulgaris (P.v.). The biopsies were obtained from freshly developed blisters along with perilesional tissue. The lymphocytic infiltrates in b.P. as well as in P.v. were located in the area of the fresh lesions and consisted almost exclusively of T cells (CD3 positive lymphocytes). In b.P., the discrepancy between a decreased number of CD2 positive lymphocytes (10-20%) and markedly higher number of CD3 staining cells (50-60% of all infiltrate cells) was striking. The characterization of the T cell subpopulations in both dermatoses showed mainly T helper cell infiltrates (CD4), while only up to 10% of T suppressor cells (CD8) were detected. CD45R positive (CD4+/CD45R+: suppression inducing) as well as CD29-positive (CD4+CD29+: cells which provide help for antibody production) T-cell subpopulations were detected in both dermatoses particularly adjacent to blister in up to 10% of the cell infiltrates. Epidermal staining with CD29 mab in b.P. up to the stratum spinosum and in P.v. within intraepidermal blisters was detected. By means of CD19 and CD21 mab B lymphocytes were minimal. Perivascular individual cell staining occurred with CD7 CD16, CD56 and CD57 mab (K/NK cells) in b.P. as well as in P.v. patients. The predominance in T cell infiltrates, particularly T helper cells, suggests the role of cellular immune mechanism in the pathogenesis of these diseases, in b.P. the CD2 antigen (SE receptor) appears to be of particular importance.
Dermatol Monatsschr 1990
PMID:[Characterization of lymphocytic infiltrate cells in bullous pemphigoid and pemphigus vulgaris]. 208 6

Blood serum alkaline phosphatase (AP) level was found elevated in the patients suffering from eczema, neurodermatitis, eczema with large skin sites involved, and in those with trophic ulcers of various origins, as against normal subjects and reference patients with sarcoidosis and Kaposi's sarcoma. Elevated level of the enzyme activity is directly related to exacerbation stage and size of the skin site involved; this level reduced after therapy and this reduction was associated with clinical improvement. No concomitant visceral abnormalities (calculous cholecystitis, liver cirrhosis, or malignant tumors) were detected in the examinees, that might influence the blood serum AP activity.
Vestn Dermatol Venerol 1990
PMID:[The alkaline phosphatase activity of the blood serum as a factor reflecting the chronic inflammatory process in the skin in generalized forms of psoriasis, neurodermatitis, eczema and trophic ulcers]. 209 93

Mitomycin C is an alkylating agent, used by intravesical instillation to treat carcinoma of the bladder. Repeated instillations can induce cystitis and an eczematous eruption affecting the palms, soles and face. If these effects are due to delayed hypersensitivity with sensitization to mitomycin C occurring in the bladder wall, it should be possible to demonstrate antigen-presenting cells in the bladder wall and positive patch tests to the drug. Using an immuno-alkaline phosphatase method we have identified CDI+ cells in bladder epithelium and submucosa and have demonstrated Birbeck granules in a few cells. In further support of our hypothesis it was also possible to demonstrate delayed type hypersensitivity in 13 out of 26 patients who had received mitomycin instillations by applying the allergen as a patch test. These results indicate that the eczematous eruption in this group of patients is most likely a hypersensitivity reaction and that it may be mediated transvesically.
Br J Dermatol 1990 Feb
PMID:Dermatitis due to intravesical mitomycin C: a delayed-type hypersensitivity reaction? 213 92

The course of serum zinc (S-Zn), plasma albumin (P-Alb), urinary zinc, serum alkaline phosphatase, and plasma alpha 2-macroglobulin levels was monitored in 14 adult hospitalized patients receiving oral glucocorticoid therapy, about 40-50 mg prednisone daily for various skin diseases. Within 3 days S-Zn decreased slightly from 12.6 +/- 2.3 mumol/liter (mean +/- SEM) to 11.1 +/- 2.5 mumol/liter. Then the level rose to about 14-15 mumol/liter and remained elevated, but within the normal range for the next 2 weeks. The P-Alb level showed parallel fluctuations although less pronounced. The S-Zn/P-Alb ratio increased from 0.024-0.029. No consistent patterns could be seen in the fluctuations occurring in the additional parameters studied. The possible role of ACTH on the S-Zn regulation is discussed.
J Invest Dermatol 1986 Jun
PMID:Serum zinc levels during oral glucocorticoid therapy. 242 19

It is now well established that epidermis, like many other tissues, contains a phospholipase A2 that is responsible for the initiation of the arachidonic acid cascade. Here we report that human epidermis also contains a second, quite distinct enzyme of the phospholipase A2 group, which is unique in its extreme activity against phospholipids in true solution. It also differs from the classic cutaneous enzyme in that (a) its activity is not reduced by pretreatment of the skin with corticosteroids in vivo nor by treatment of the epidermal homogenate with alkaline phosphatase in vitro, and (b) its activity is reduced, rather than increased, in the lesions of inflammatory diseases such as psoriasis. The enzyme seems to occur mainly in fully differentiated keratinocytes, its level being low in the basal cell layer of epidermis and in keratinocytes cultured in vitro. On the basis of these observations, we suggest that this new phospholipase A2 is responsible for the degradation of phospholipids that accompanies the terminal keratinization process.
J Invest Dermatol 1988 Jan
PMID:A unique phospholipase A2 in human epidermis: its physiologic function and its level in certain dermatoses. 244 92


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>